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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Chronic kidney disease (CKD) affects over 10% of adults worldwide and is a major cause of morbidity and mortality. Albuminuria and proteinuria are established prognostic markers but insufficiently reflect tubular and interstitial injury. Fetuin-A is a liver-derived glycoprotein regulating calcium-phosphate balance and inflammation. In CKD and dialysis patients, low serum Fetuin-A is linked to cardiovascular events and mortality but is easily influenced by inflammation and nutrition. In contrast, urinary post-translationally modified Fetuin-A (uPTM-FetA) fragments reflect tubular injury and fibrosis and show better predictive value for renal decline in diabetic and graft kidney disease than albuminuria. However, evidence in non-diabetic CKD and its link with long-term outcomes remains limited. This study evaluated whether urinary uPTM-FetA/creatinine ratio (UFC) predicts renal outcomes and mortality in CKD stages 2–4.
We conducted a prospective observational cohort of 139 adults (≥20 years) with CKD stages 2–4 at National Cheng Kung University Hospital from July 2019 to October 2022. uPTM-FetA was quantified by DNlite® IVD103 ELISA (Bio Preventive Medicine Corp., Taiwan) and expressed as UFC (ng/mg). The primary endpoints were (1) a combined renal and mortality outcome, defined as all-cause death, sustained eGFR <10 mL/min/1.73 m², ≥40% eGFR decline, or initiation of dialysis/kidney transplantation, and (2) all-cause mortality. The secondary endpoint was the renal composite outcome. Patients were followed for a median of 3.17 years (IQR 2.89–6.11). Kaplan–Meier and Cox regression analyses estimated event-free survival and hazard ratios (HRs) with 95% confidence intervals (CIs).
Mean age was 67.5 ± 11.9 years, baseline eGFR 31.9 ± 11.4 mL/min/1.73 m²; 27% had diabetes and 67% hypertension. Median UFC was 14.91 ng/mg. During follow-up, 59 patients (42%) had the primary combined outcome, including 13 deaths, 17 dialysis initiations, and 34 with sustained eGFR <10 mL/min/1.73 m²; 53 (38%) met the renal composite alone. Compared with the low UFC group (<14.91 ng/mg, n=65), the high UFC group (≥14.91 ng/mg, n=74) had poorer event-free survival (58.0 ± 3.1 vs. 66.9 ± 2.6 months; log-rank p=0.025). In univariate Cox models, high UFC predicted the combined outcome (HR 2.12, 95% CI 1.23–3.63, p=0.006) and the renal composite (HR 2.28, 95% CI 1.09–4.76, p=0.029). After adjustment for age, sex, and baseline eGFR, high UFC remained an independent predictor of the primary combined outcome (adjusted HR 2.05, 95% CI 1.18–3.55, p=0.011) and all-cause mortality (adjusted HR 4.08, 95% CI 1.07–15.55, p=0.039), while the secondary renal composite showed a similar but non-significant trend (HR 1.83, p=0.115). Baseline eGFR was a consistent protective factor (p<0.01).
Higher urinary uPTM-FetA/creatinine ratio (UFC) was independently associated with increased risks of the combined renal and mortality outcome and all-cause mortality in CKD stages 2–4. Reflecting tubular hypoxia and fibrosis, UFC may serve as a sensitive, non-invasive biomarker for early risk stratification and prognosis in CKD.
